Intradural lumbar disc herniation. Report of three cases with a review of the literature

Intradural lumbar disc herniation (ILDH) is rare. Three new cases of this condition are reported, adding to the 70 previously documented cases. An incidence of ILDH in between 0.04 and 0.33 percent of lumbar disc protrusions has been reported. More than one third of ILDH were observed at L1-2 to L3-4 levels, while only a tenth of cases occurred at L5-S1. The mechanism of ILDH is not known with certainty. Adhesions between the ventral wall of the dura and posterior longitudinal ligament could act as a preconditioning factor. A diagnosis of ILDH may be made with difficulty, and it is seldom suspected preoperatively. Prompt surgery is necessary because the neurologic prognosis appears to be closely linked with preoperative duration of neurologic symptoms.     

Neurotoxicity induced by tacrolimus after liver transplantation: relation to genetic polymorphisms of the ABCB1 (MDR1) gene

BACKGROUND: Tacrolimus is a substrate of P-glycoprotein (PGP) encoded by the multidrug resistant (MDR)1 gene (ABCB1). PGP, a multidrug efflux pump, restricts the distribution of tacrolimus in the brain. In this study, we investigate the correlation of ABCB1 gene polymorphism with tacrolimus-induced neurotoxicity in patients after liver transplantation. METHODS: The genotype of 6 patients with neurotoxic events and 11 patients without neurotoxic events was analyzed by polymerase chain reaction (PCR), and 8 mutations were detected. In addition to laboratory findings and patient characteristics, the contribution of mutations in the ABCB1 gene was evaluated with stepwise discriminant function analysis. RESULTS: High tacrolimus concentration, liver dysfunction, and mutation at position 2677 in exon 21 were demonstrated as positive predictors of tacrolimus-induced neurotoxicity. CONCLUSION: It is indicated that blood concentrations, liver function, graft weight, and polymorphism in the ABCB1 gene are important factors in tacrolimus-induced neurotoxicity.     

Lung resection affects the postoperative arrhythmia and electrocardiographic axis deviation]

After lung lobectomy or pneumonectomy, the mediastinal shift and diaphragmatic elevation are occurred. Because this phenomenon may affect the heart positional change, we studied the electrocardiographic QRS axis in the frontal plane (from leads I and III) and the postoperative arrhythmia. Seventy three patients who had no heart disease including arrhythmia before the surgery were recorded their electrocardiogram (ECG) before their surgery and after their discharge. When the postoperative ECG was recorded, they had no respiratory failure nor cancer recurrence, and their lungs were fully expanded in their thoracic cages. After right upper lobectomy (19 cases), the axis was twisted rightward slightly (2.1 degrees). Right middle lobectomy (2 cases, 9.5 degrees) and right upper and middle lobectomies (3 cases, 7.3 degrees) twisted the heart axes more rightwards. Right lower lobectomy (12 cases, -1.0 degree) and right middle and lower lobectomies (3 cases, -17.7 degrees) contorted their axes leftwards and right pneumonectomy (5 cases, 31.4 degrees) rightwards. The axes were turned rightwards after the left upper lobectomy (18 cases, 2.8 degrees) and the left lower lobectomy (7 cases, 3.9 degrees). Left pneumonectomy (4 cases, -4.0 degrees) twisted the axis leftwards. After the surgery, arrhythmias were recorded in 14 cases and, among these patients, 5 cases were required the oral anti-arrhythmic medication. Most of these cases changed their heart axes after the surgery and it is suggested that the axial deviation may contribute to their postoperative arrhythmia.     

Risk factors and prediction of bleeding after gastric endoscopic submucosal dissection in patients on antithrombotic therapy: newly developed bleeding prediction application software,SAMURAI model

Bleeding after gastric endoscopic submucosal dissection (ESD) remains problematic, especially in patients receiving antithrombotic therapy. Therefore, this study aimed to identify the risk factors. In this retrospective study, patients (n = 1,207) who underwent gastric ESD while receiving antithrombotic therapy were enrolled at Osaka Medical and Pharmaceutical University Hospital and 18 other referral hospitals in Japan. Risks of post-ESD bleeding were calculated using multivariable logistic regression. The dataset was divided into a derivation cohort and a validation cohort. We created a prediction model using the derivation cohort. The accuracy of the model was evaluated using the validation cohort. Post-ESD bleeding occurred in 142 (11.8%) participants. Multivariable analysis yielded an odds ratio of 2.33 for aspirin, 4.90 for P2Y12 receptor antagonist, 1.79 for cilostazol, 0.95 for other antithrombotic agents, 6.53 for warfarin, 5.65 for dabigatran, 7.84 for apixaban, 10.45 for edoxaban, 6.02 for rivaroxaban, and 1.46 for heparin bridging. The created prediction model was called safe ESD management using the risk analysis of post-bleeding in patients with antithrombotic therapy (SAMURAI). This model had good predictability, with a C-statistic of 0.77. In conclusion, use of the SAMURAI model will allow proactive management of post-ESD bleeding risk in patients receiving antithrombotic therapy.     

Effect of retinoic acid on osteopontin expression in rat clonal dental pulp cells

We studied the effect of retinoic acid on osteopontin synthesis and the mRNA expression in rat clonal dental pulp cells, RPC-C2A. An immunoprecipitation assay clarified that retinoic acid caused an increase in phosphorylated osteopontin synthesis that was dose-dependent, and marked increases were observed at retinoic acid concentrations of 10(-6) to 10(-5) M (1.7-fold). A Northern blotting analysis revealed a similar pattern of increase in osteopontin mRNA expression of up to 6.2-fold of control levels. Because osteopontin has an important role in the mineralization process, these results suggest that retinoic acid regulates mineralization, which takes place in the pulp cavity, including reparative dentin formation.     

Enhanced tumor growth and invasiveness in vivo by a carboxyl-terminal fragment of alpha1-proteinase inhibitor generated by matrix metalloproteinases: a possible modulatory role in natural killer cytotoxicity

Matrix metalloproteinases (MMPs) are believed to contribute to the complex process of cancer progression. They also exhibit an alpha1-proteinase inhibitor (alphaPI)-degrading activity generating a carboxyl-terminal fragment of approximately 5 kd (alphaPI-C). This study reports that overexpression of alphaPI-C in S2-020, a cloned subline derived from the human pancreas adenocarcinoma cell line SUIT-2, potentiates the growth capability of the cells in nude mice. After stable transfection of a vector containing a chimeric cDNA encoding a signal peptide sequence of tissue inhibitor of metalloproteinase-1 followed by cDNA for alphaPI-C into S2-020 cells, three clones that stably secrete alphaPI-C were obtained. The ectopic expression of alphaPI-C did not alter in vitro cellular growth. However, subcutaneous injection of the alphaPI-C-secreting clones resulted in tumors that were 1.5 to 3-fold larger than those of control clones with an increased tendency to invasiveness and lymph node metastasis. These effects could be a result of modulation of natural killer (NK) cell-mediated control of tumor growth in nude mice, as the growth advantage of alphaPI-C-secreting clones was not observed in NK-depleted mice, and alphaPI-C-secreting clones showed decreased NK sensitivity in vitro. In addition, production of alphaPI and generation of the cleaved form of alphaPI by MMP were observed in various human tumor cell lines and in a highly metastatic subline of SUIT-2 in vitro. These results provide experimental evidence that the alphaPI-degrading activity of MMPs may play a role in tumor progression not only via the inactivation of alphaPI but also via the generation of alphaPI-C.